A 48-year-old woman with severe mitral stenosis and severe pulmonary hypertension undergoes percutaneous balloon mitral valvuloplasty — and returns with severe mitral regurgitation, pulmonary edema, and a right heart under pressure.
A 48-year-old woman presented with three months of exertional breathlessness that resolved with rest. She had no chest pain, no palpitations, no orthopnoea, no oedema. She was not hypertensive, not diabetic, had no history of stroke or coronary disease. She had never smoked. Her ECG showed T-wave inversions in leads III, aVF, and V2–V6. Her echocardiogram told a different story: severe mitral stenosis, severe pulmonary hypertension, and a right heart under pressure.
The plan was percutaneous balloon mitral valvuloplasty (PBMV). The balloon crossed the valve, dilated it — and something went wrong. The V wave shot up. Severe mitral regurgitation. Pulmonary oedema. The patient was shifted for emergency mitral valve replacement (MVR). This case is about the right heart, the pulmonary circulation, and the anaesthetic battle to keep both alive.
The ECG showed T-wave inversions in leads III, aVF and V2–V6. These changes are non-specific. In a patient with severe pulmonary hypertension they are commonly attributed to right ventricular strain, and the echo findings (dilated RV, D-shaped LV) fit that picture. There were no arrhythmias, and coronary angiography showed normal epicardial coronaries, so an ischaemic cause was not supported.
The pre-procedure TTE and TEE tell the same story with slightly different numbers. The difference between them is worth noting: gradients depend on heart rate and flow, while planimetry does not.
| Parameter | TTE | TEE | What it means |
|---|---|---|---|
| MVA, planimetry | 1.2 cm² | 1.4 cm² | Direct trace of the orifice, independent of rate and flow. Severe MS is ≤1.5 cm². |
| MVA, PHT | — | 1.1 cm² | 220 ÷ pressure half-time. Concordant with planimetry. |
| Mitral gradient | 27 / 10 mmHg | 21 / 16 mmHg | Flow- and rate-dependent, so it varies between studies. |
| Leaflets and subvalvular apparatus | — | AML doming, PML restricted; subvalvular grade 3 | Classic rheumatic MS. Grade 3 subvalvular disease lowers the odds of a clean PBMV result. |
| MR / AR | Mild / Mild | Mild / Mild (AR jet 20% of LVOT, PHT 670 ms) | Baseline MR was mild, which gives a reference for comparison after PBMV. |
| TR and PA pressure | Severe TR · RVSP 70 mmHg | Severe TR, dilated annulus · TR velocity 5.08 m/s · PASP ~100 mmHg | Functional TR (dilated annulus). 4v² ≈ 103 mmHg, plus RA pressure, implies near-systemic pulmonary pressure. |
| RA / RV / septum | Dilated | Dilated · D-shaped LV | Septal flattening reflects RV pressure and/or volume overload and can impair LV filling. |
| LV | EF 58%, no RWMA | Good systolic function | Preserved systolic function. The LV is under-filled because of the mitral obstruction rather than intrinsically weak. |
| LA / LAA | No clot on 2D | SEC · organic LAA clot · LAA velocity 38 cm/s | Spontaneous echo contrast reflects stasis. LAA emptying velocity of 38 cm/s is reduced (normally above about 40–50 cm/s). |
Four components, each graded 1–4 (maximum 16). A score of 8 or less predicts a good PBMV result, 9–11 is borderline, and higher scores predict a less favourable result.
M3 and S3 describe a valve whose commissures can be opened but whose leaflets and chordae cannot stretch to accommodate it. Splitting the commissure can then tear a leaflet or rupture a chord. The total score estimates the likelihood of a good result, and the sub-score pattern can hint at how an unfavourable result might arise.
Severe MS is not just a valve problem — it is a haemodynamic cascade that affects the left atrium, pulmonary circulation, right heart, and eventually the left ventricle.
In severe MS with severe PAH, the right ventricle is the vulnerable chamber. It is pressure-loaded, dilated, and poorly tolerant of any additional afterload increase. Anaesthetic management centres on protecting the RV: maintaining systemic perfusion pressure, avoiding hypoxia, hypercarbia and acidosis, preserving sinus rhythm, and using inotropes and pulmonary vasodilators judiciously.
Severe pulmonary hypertension (RVSP ~70–100 mmHg) in this patient was a major determinant of risk and the central challenge for anaesthetic management.
A D-shaped LV on TEE indicates RV pressure and/or volume overload, with the septum flattened toward the LV cavity. It is a marker of significant RV strain and a reason to anticipate haemodynamic difficulty, particularly during induction and weaning from bypass.
Percutaneous balloon mitral valvuloplasty (PBMV) is a catheter-based procedure that dilates the stenotic mitral valve using a balloon. The standard technique is the Inoue balloon, which is advanced from the femoral vein, across the interatrial septum, into the left atrium, and then across the mitral valve into the left ventricle.
Post-PBMV, the patient developed severe mitral regurgitation. The V wave on left atrial pressure tracing rose to ~75–80 mmHg — a giant V wave indicating severe MR. The patient developed pulmonary oedema and was shifted for emergency MVR.
| Parameter | Pre-PBMV | Post-PBMV |
|---|---|---|
| LA mean pressure | 24 mmHg | Not recorded |
| V wave | 34 mmHg | 75–80 mmHg |
| LVEDP | 0–6 mmHg | — |
| Mitral gradient | 18 mmHg | — |
| Mitral regurgitation | Mild | Severe |
| Clinical status | Stable | Pulmonary oedema |
Chronic MR is tolerated because the LA enlarges and becomes compliant. Here the LA was pressure-loaded and poorly compliant from long-standing stenosis, and had not adapted to absorb a regurgitant volume. The V wave is then transmitted to the pulmonary veins, producing oedema in a lung bed and RV already under high pressure. The stenosis had developed over years, whereas the regurgitation appeared within minutes.
The exact mechanism of the MR is not established here. Features that are recognised predictors of severe MR or a suboptimal result after PBMV, and that this patient had, include:
Severe MR can follow PBMV even in apparently suitable valves, so these features raise the likelihood without making the outcome certain. Severe PAH did not cause the MR, but it made the sudden regurgitant volume much harder to tolerate.
After PBMV, the patient developed severe MR with pulmonary oedema. Medical management was insufficient, and the decision was made to proceed with emergency mitral valve replacement (MVR) on cardiopulmonary bypass.
Any MVR is demanding. This one stacked four independent problems on a single circulation.
Added to these were the risk of coagulopathy after bypass and the likely need for postoperative ventilation.
The patient was shifted to the cardiac operating room with continuous monitoring. With severe PAH and a mixed mitral lesion, the goals were:
The aim is haemodynamic stability: no fall in SVR, no rise in PVR, no tachycardia. Agents commonly used include etomidate (minimal haemodynamic effect) and opioids such as fentanyl, titrated slowly. Ketamine has little direct effect on PVR when ventilation is controlled, but its tachycardia is a drawback. Propofol needs caution because of vasodilation and hypotension.
The patient was induced with a carefully titrated technique and ventilated with a lung-protective strategy: modest tidal volumes, PEEP to avoid derecruitment, and enough FiO₂ to avoid hypoxia. Hypercarbia was avoided, since it raises PVR and can precipitate RV failure.
An intercostal nerve block was performed for intraoperative and postoperative analgesia. This reduces opioid requirements and improves pain control. In a patient with severe PAH, adequate analgesia matters because pain increases sympathetic tone and PVR.
Bypass itself will be covered in a separate case, so only the points relevant here are included. The patient was heparinised to an ACT above 480 seconds (540 seconds achieved) and placed on CPB, and the mitral valve was replaced under cardioplegic arrest. Weaning was the high-risk moment: the RV, unloaded during bypass, had to eject again against a high pulmonary vascular resistance, and was supported with inotropes and vasopressors under TEE guidance.
Heparin was reversed with protamine, with a post-protamine ACT of 105 seconds. In severe PAH protamine is best given slowly with a vasopressor ready, because of the risk of pulmonary vasoconstriction. Blood products, including FFP, were given as guided by bleeding, ABG and coagulation results.
| Drug | Class / Mechanism | Role in this case |
|---|---|---|
| Noradrenaline | α1 agonist with some β1 effect → ↑SVR | Maintains systemic pressure and coronary perfusion of the RV. |
| Dopamine | Dose-dependent: β1 inotrope, α1 vasopressor | Inotropic support. |
| Adrenaline | α + β agonist → ↑HR, ↑contractility, ↑SVR | Additional inotropic and vasopressor support for RV or LV dysfunction. |
| Milrinone | PDE3 inhibitor → ↑contractility, ↓SVR, ↓PVR | RV support and pulmonary vasodilation. Its systemic vasodilation is why it is often paired with noradrenaline. |
At the end of the procedure, the patient remained intubated and was shifted to the ICU with full inotropic and vasopressor support (noradrenaline, dopamine, adrenaline, and milrinone). Reasons that commonly favour continued ventilation in this setting include:
The pulmonary circulation remained reactive, and hypoxia, hypercarbia, pain or light sedation could provoke a pulmonary hypertensive crisis.
The RV was dilated and pressure-loaded. It needed inotropic support (milrinone, adrenaline) and careful preload management. Hypoxia, hypercarbia or agitation during emergence could raise PVR, whereas controlled ventilation allows tight control of oxygenation and CO₂.
Pulmonary oedema had developed from acute severe MR, and PEEP and positive pressure ventilation support oxygenation while the lungs recover.
Myocardial stunning after bypass is common, and inotropic support was needed to maintain cardiac output.
Bypass causes dilutional coagulopathy and platelet dysfunction. The patient received blood and FFP, and early extubation is generally avoided while bleeding risk remains.
Bleeding or tamponade may require a return to theatre, and an intubated, sedated patient can be transferred and monitored safely.
Dilated, pressure-loaded RV on a dropping systemic pressure. The first sign is a rising CVP with a falling MAP. Treat the cause: oxygenate, ventilate, inotrope, vasopressor, and consider inhaled pulmonary vasodilator.
Triggered by light anaesthesia, suction, hypoxia, hypercarbia, acidosis, or protamine. Prevent with depth, oxygenation, ventilation, and slow protamine.
Once the regurgitant leak is closed, the LV faces a higher afterload. Inotropic support and volume optimisation are the usual responses.
An uncommon but catastrophic early complication of MVR. Warning signs are sudden haemorrhage and a pressure drop after weaning.
Already present from the acute MR. PEEP, lung-protective ventilation and fluid restraint after bypass.
Heparin effect, dilutional coagulopathy and platelet dysfunction after bypass. Blood products guided by ACT, coagulation tests and visible bleeding.
Atrial fibrillation with loss of atrial kick is poorly tolerated in a valve-replaced heart. Maintain electrolytes, magnesium, and rate control.
Low SVR after bypass. Noradrenaline first, with vasopressin as a second-line option.
This case is a study in right heart physiology and pulmonary vascular control. The left-sided valve was the trigger, but the right heart set the limits. The sudden regurgitant volume fell on an already compromised pulmonary circulation, and the anaesthetic had to hold a narrow path between systemic hypotension and pulmonary hypertensive crisis.
A Wilkins score of 9 with grade 3 subvalvular disease raises the likelihood of leaflet injury and significant MR, and severe MR is a recognised complication of PBMV. The case is also a reminder that the lesion can change during a procedure, and the plan has to change with it: stenotic physiology was replaced by regurgitant physiology in a lung bed already under high pressure.
Management was layered: noradrenaline for systemic pressure, milrinone for RV inotropy and pulmonary vasodilation, dopamine and adrenaline as further support, and careful heparin and protamine management. Continued ventilation afterwards gave the right heart time to recover.
Ode to the OR is a personal project dedicated to education and reflection. Any patient-related content has been fully de-identified and may be modified to protect confidentiality in accordance with HIPAA principles, the Digital Personal Data Protection (DPDP) Act, 2023 (India), and the ethical mandates of the National Medical Commission (NMC) of India. Patient age, procedural details, haemodynamic values and timeline elements have been generalised where necessary. The pressure tracings and circulation diagram shown are schematic illustrations, not the patient's recorded waveforms. AI tools may assist with language refinement and presentation, but all content is reviewed, curated, and published by the author. The views expressed are solely my own and do not represent any institution, hospital, employer, or training program. Nothing on this site should be considered medical advice or a substitute for professional clinical judgment.